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Virology. 2014 Jan 20;449:270-86. doi: 10.1016/j.virol.2013.11.023. Epub 2013 Dec 15.

Reactive oxygen species activate NFκB (p65) and p53 and induce apoptosis in RVFV infected liver cells.

Author information

1
National Center for Biodefense and Infectious Diseases, and the School of Systems Biology, George Mason University, Manassas, VA, USA.
2
Center for Applied Proteomics and Personalized Medicine, George Mason University, Manassas, VA, USA.
3
George Washington Medical School, Washington DC, USA.
4
United States Army Medical Research Institute for Infectious Diseases, Fredrick, MD, USA.
5
National Center for Biodefense and Infectious Diseases, and the School of Systems Biology, George Mason University, Manassas, VA, USA. Electronic address: fkashanc@gmu.edu.

Abstract

Rift Valley fever virus (RVFV) infection is often associated with pronounced liver damage. Previously, our studies revealed altered host phospho-signaling responses (NFκB, MAPK and DNA damage responses) in RVFV infected epithelial cells that correlated with a cellular stress response. Here, we report that RVFV infection of liver cells leads to an increase in reactive oxygen species (ROS). Our data suggests the presence of the viral protein NSs in the mitochondria of infected cells, hence contributing to early increase in ROS. Increased ROS levels correlated with activation of NFκB (p65) and p53 responses, which in conjunction with infection, was also reflected as macromolecular rearrangements observed using size fractionation of protein lysates. Additionally, we documented an increase in cytokine expression and pro-apoptotic gene expression with infection, which was reversed with antioxidant treatment. Collectively, we identified ROS and oxidative stress as critical contributors to apoptosis of liver cells during RVFV infection.

KEYWORDS:

Apoptosis; Liver cells; Reactive oxygen species; Rift Valley fever virus; p53; p65

PMID:
24418562
DOI:
10.1016/j.virol.2013.11.023
[Indexed for MEDLINE]
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